Rosenberger (mathematics and information, college of Maryland) and Lachin (biostatistics and information, George Washington collage) mix utilized points of randomization in scientific trials with a probabilistic therapy of homes of randomization during this text/reference for biostatistics graduate scholars and biostatisticians in perform.

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Both PDGF and FGF can act as chemotactic agents for SMC, and there also appears to be a SMC-derived factor that acts as an autoregulatory agent that mediates SMC migration (218). During migration, SMC do not appear to proliferate, but on arrival in the intima, many of the SMC begin another phase of cell division (202). Thus, there are two stages of proliferation involved in neointimal formation, the initial dedifferentiation of SMC followed by proliferation within the media, and a second proliferative stage after migration into the intima has occurred.

SMC from injured arteries secrete only the PDGF-AA despite expressing the genes for both chains (184). Yet the receptor type that is expressed in these SMC is the βreceptor (185). It is uncertain why these cells would express one ligand and another type of receptor. The answer may be that different isoforms are generated for different functions with different target cells. Injury to the artery also exposes the underlying SMC to circulating platelets, which have been shown to adhere to the injured vessel, as well as being a source of PDGF-BB (186).

VI. DETERMINANTS OF PLAQUE STABILITY Atherosclerosis results in the development of various symptoms, depending on the vascular bed that is affected (9). The most signiﬁcant and potentially lethal manifestations of atherosclerosis are the development of unstable angina, myocardial infarction, or cerebral vascular ischemia, which can result from plaque rupture with thrombus formation (98). Understanding the determinants of plaque stability and factors that can lead to instability and rupture of a plaque is crucial in preventing these complications of atherosclerosis.